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Manolis Kellis

Researcher at Massachusetts Institute of Technology

Publications -  448
Citations -  132627

Manolis Kellis is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Gene & Genome. The author has an hindex of 128, co-authored 405 publications receiving 112181 citations. Previous affiliations of Manolis Kellis include Broad Institute & Epigenomics AG.

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Network Infusion to Infer Information Sources in Networks

TL;DR: This paper introduces a method called Network Infusion (NI), designed to circumvent issues of source inference practical for large, complex real world networks, and proposes an integrative source inference framework that combines NI with a distance centrality-based method, which leads to a robust performance in cases where the underlying dynamics are unknown.
Posted ContentDOI

Functional enrichments of disease variants across thousands of independent loci in eight diseases

TL;DR: This work uses epigenomic annotations across 127 tissues and cell types to investigate weak regulatory associations, the specific enhancers they reside in, their downstream target genes, their upstream regulators, and the biological pathways they disrupt in eight common diseases.
Posted ContentDOI

A Bayesian approach to mediation analysis predicts 206 causal target genes in Alzheimer’s disease

TL;DR: Causal Multivariate Mediation within Extended Linkage disequilibrium is developed, a novel Bayesian inference framework to jointly model multiple mediated and unmediated effects relying only on summary statistics, and it is shown in simulation that CaMMEL accurately distinguishes between mediating and pleiotropic genes unlike existing methods.
Posted ContentDOI

RiVIERA-beta: Joint Bayesian inference of risk variants and tissue-specific epigenomic enrichments across multiple complex human diseases

TL;DR: A new Bayesian model RiVIERA-beta (Risk Variant Inference using Epigenomic Reference Annotations) is introduced for inference of driver variants by modelling summary statistics p-values in Beta density function across multiple traits using hundreds of epigenomic annotations to model GWAS summary statistics of 9 autoimmune diseases and Schizophrenia.